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Knockout mice reveal a contribution of the extracellular matrix molecule tenascin-C to neural precursor proliferation and migration

Emmanuel Garcion¹, Andreas Faissner^2,* and Charles ffrench-Constant^1,

¹ Department of Medical Genetics and Cambridge Center for Brain Repair, University of Cambridge, The E.D. Adrian Building, Forvie Site, Robinson Way, Cambridge CB2 2PY, UK
² Centre de Neurochimie du CNRS, Laboratoire de Neurobiologie du Développement et de la Régénération, UPR 1352, 5 rue Blaise Pascal, 67084 Strasbourg Cedex, France
^* Present address: Department of Molecular Neurobiology, Ruhr University, Building NDEF 05/593, Universitaetsstr. 150, D44801, Bochum, Germany

Author for correspondence (e-mail: cfc{at}mole.bio.cam.ac.uk)

Accepted April 12, 2001

The extracellular matrix glycoprotein tenascin-C is widely expressed in the vertebrate central nervous system (CNS) during development and repair. Despite multiple effects of tenascin-C on cell behaviour in culture, no structural abnormalities of the CNS and other organs have been found in adult tenascin-C-null mice, raising the question of whether this glycoprotein has a significant role in vivo. Using a transgenic approach, we have demonstrated that tenascin-C regulates both cell proliferation and migration in oligodendrocyte precursors during development. Knockout mice show increased rates of oligodendrocyte precursor migration along the optic nerve and reduced rates of oligodendrocyte precursor proliferation in different regions of the CNS. Levels of programmed cell death were reduced in areas of myelination at later developmental stages, providing a potential corrective mechanism for any reduction in cell numbers that resulted from the proliferation phenotype. The effects on cell proliferation are mediated via the vß3 integrin and an interaction with the platelet-derived growth factor-stimulated mitogenic pathway, emphasising the importance of both CNS extracellular matrix and integrin growth factor interactions in the regulation of neural precursor behaviour.

Key words: Tenascin-C, vß3, Integrin, Proliferation, Central nervous system, Migration, Apoptosis, Mouse

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